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1.
Artigo em Inglês | MEDLINE | ID: mdl-21144004

RESUMO

Our understanding of the pathogenesis of "tendinopathy" is based on fragmented evidences like pieces of a jigsaw puzzle. We propose a "failed healing theory" to knit these fragments together, which can explain previous observations. We also propose that albeit "overuse injury" and other insidious "micro trauma" may well be primary triggers of the process, "tendinopathy" is not an "overuse injury" per se. The typical clinical, histological and biochemical presentation relates to a localized chronic pain condition which may lead to tendon rupture, the latter attributed to mechanical weakness. Characterization of pathological "tendinotic" tissues revealed coexistence of collagenolytic injuries and an active healing process, focal hypervascularity and tissue metaplasia. These observations suggest a failed healing process as response to a triggering injury. The pathogenesis of tendinopathy can be described as a three stage process: injury, failed healing and clinical presentation. It is likely that some of these "initial injuries" heal well and we speculate that predisposing intrinsic or extrinsic factors may be involved. The injury stage involves a progressive collagenolytic tendon injury. The failed healing stage mainly refers to prolonged activation and failed resolution of the normal healing process. Finally, the matrix disturbances, increased focal vascularity and abnormal cytokine profiles contribute to the clinical presentations of chronic tendon pain or rupture. With this integrative pathogenesis theory, we can relate the known manifestations of tendinopathy and point to the "missing links". This model may guide future research on tendinopathy, until we could ultimately decipher the complete pathogenesis process and provide better treatments.

2.
J Orthop Surg Res ; 3: 7, 2008 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-18289375

RESUMO

BACKGROUND: Excessive pronation (or eversion) at ankle joint in heel-toe running correlated with lower extremity overuse injuries. Orthotics and inserts are often prescribed to limit the pronation range to tackle the problem. Previous studies revealed that the effect is product-specific. This study investigated the effect of medial arch-heel support in inserts on reducing ankle eversion in standing, walking and running. METHODS: Thirteen pronators and 13 normal subjects participated in standing, walking and running trials in each of the following conditions: (1) barefoot, and shod condition with insert with (2) no, (3) low, (4) medium, and (5) high medial arch-heel support. Motions were captured and processed by an eight-camera motion capture system. Maximum ankle eversion was calculated by incorporating the raw coordinates of 15 anatomical positions to a self-compiled Matlab program with kinematics equations. Analysis of variance with repeated measures with post-hoc Tukey pairwise comparisons was performed on the data among the five walking conditions and the five running conditions separately. RESULTS: Results showed that the inserts with medial arch-heel support were effective in dynamics trials but not static trials. In walking, they successfully reduced the maximum eversion by 2.1 degrees in normal subjects and by 2.5-3.0 degrees in pronators. In running, the insert with low medial arch support significantly reduced maximum eversion angle by 3.6 and 3.1 degrees in normal subjects and pronators respectively. CONCLUSION: Medial arch-heel support in inserts is effective in reducing ankle eversion in walking and running, but not in standing. In walking, there is a trend to bring the over-pronated feet of the pronators back to the normal eversion range. In running, it shows an effect to restore normal eversion range in 84% of the pronators.

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